Li Yilin, Wang Tingting, Ma Beibei, Yu Shangyue, Pei Hailuan, Tian Shiqiu, Tian Yingying, Liu Chuang, Zhao Xinyue, Zuo Zeping, Wang Zhibin
School of Chinese Pharmacy, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Beijing Tongrentang Technology Co., LTD. Pharmaceutical Factory, Beijing, People's Republic of China.
J Inflamm Res. 2023 Sep 28;16:4331-4346. doi: 10.2147/JIR.S423240. eCollection 2023.
Xianglian Zhixie Tablet (XLZXT), a classical traditional Chinese medicine formulation, is commonly used to treat Ulcerative Colitis (UC) in China. However, the therapeutic mechanisms of XLZXT for UC have yet to be fully understood. This study aimed to investigate the curative benefits of XLZXT and its associated mechanisms for healing UC in mice.
In the present study, the 1% dextran sulfate sodium (DSS) solution was used to establish the UC model in C57BL/6N mice. To investigate the therapeutic effects of XLZXT on DSS-induced UC mice, several parameters were measured, including DAI score, colon length, spleen index, pathological changes in colon tissue, and levels of inflammatory factors in plasma and colon tissue. By investigating the gut microbiota, assessing the levels of intestinal mucosal protein expression, and looking at the proteins involved in the TLR4/MyD88/NF-B p65 signaling pathway, the mechanisms of XLZXT impact on UC were investigated. Mouse feces were examined for patterns of gut microbiota expression using high-throughput sequencing of 16S rRNA.
XLZXT effectively alleviated UC symptoms and colon pathological damage in DSS-induced UC mice. It improved body weight loss, stool consistency, and hematochezia, while also repairing colon damage. Moreover, it down-regulated pro-inflammatory cytokines (such as TNF-α, IL-1β, and IL-6), and up-regulated anti-inflammatory cytokines (such as IL-10). XLZXT also increased the expression of MUC-2, Occludin and ZO-1, while decreasing the expression of NF-κB, MyD88 and TLR4. Additionally, it regulated gut microbiota disorder by increasing the abundance of beneficial bacteria and reducing the adhesion of intestinal harmful bacteria.
XLZXT demonstrated therapeutic effects on DSS-induced UC mice. The mechanisms may be associated with repairing the intestinal mucosal barrier, regulating the TLR4/MyD88/NF-κB p65 signaling pathway, and restoring the balance of gut microbiota.
香连止泻片（XLZXT）是一种经典的中药制剂，在中国常用于治疗溃疡性结肠炎（UC）。然而，XLZXT治疗UC的机制尚未完全明确。本研究旨在探讨XLZXT对小鼠UC的治疗效果及其相关机制。
在本研究中，使用1%葡聚糖硫酸钠（DSS）溶液在C57BL/6N小鼠中建立UC模型。为了研究XLZXT对DSS诱导的UC小鼠的治疗效果，测量了几个参数，包括疾病活动指数（DAI）评分、结肠长度、脾脏指数、结肠组织的病理变化以及血浆和结肠组织中炎症因子的水平。通过研究肠道微生物群、评估肠黏膜蛋白表达水平以及观察参与Toll样受体4（TLR4）/髓样分化因子88（MyD88）/核因子κB（NF-κB）p65信号通路的蛋白，探讨了XLZXT对UC影响的机制。使用16S核糖体RNA（rRNA）高通量测序检查小鼠粪便中肠道微生物群的表达模式。
XLZXT有效减轻了DSS诱导的UC小鼠的UC症状和结肠病理损伤。它改善了体重减轻、粪便稠度和便血情况，同时还修复了结肠损伤。此外，它下调了促炎细胞因子（如肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）），并上调了抗炎细胞因子（如白细胞介素-10（IL-10））。XLZXT还增加了黏蛋白-2（MUC-2）、闭合蛋白（Occludin）和紧密连接蛋白1（ZO-1）的表达，同时降低了NF-κB, MyD88和TLR4的表达。此外，它通过增加有益菌的丰度和减少肠道有害菌的黏附来调节肠道微生物群紊乱。
XLZXT对DSS诱导的UC小鼠具有治疗作用。其机制可能与修复肠黏膜屏障、调节TLR4/MyD88/NF-κB p65信号通路以及恢复肠道微生物群平衡有关。
